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Demilienizing diseases of the nervous system. Etiology, pathogenesis, clinical forms of diseases

DEMIELINIZING DISEASES.

The main pathological manifestation is the selective destruction of the myelin sheath.

Myelin:

- in the central nervous system - oligodendrocyte

- in the PNS - lemmocyte (Schwann cells)

The thicker the myelin sheath, the faster the anterior nerve impulse.

Demyelinating diseases:

- multiple sclerosis

- acute disseminated encephalomyelitis

- retrobulbar neuritis

- concentric sclerosis (Balo)

- Diffuse sclerosis (Schilder's disease)

- Otry and subacute hemorrhagic. Leukoencephalitis

- optoneuromyelitis (Devic's disease)

- Demyelinizir.forms of polyneuropathy (Guillain-Barré syndrome)

Multiple sclerosis - chronic progressive disease of the central nervous system and manifested. diffuse (multi-focal) neurological symptoms and having, in typical cases, early stages of remmitir. Flow. Observed more often in young people (20-40 years old) and leads to severe disability.

History of the study of multiple sclerosis:

1835 Crewellier described islet sclerosis

In 1868, Sharko described the clinical manifestations of the disease.

Epidemiology of MS:

1. High-risk zone - the northern regions of Europe and the USA, the south of Canada and Australia, Russia and New Zealand.

2. The medium-risk zone (10-50 cases per 100,000 population) - southern Europe and the USA, northern Africa and Australia

3. Low-risk zone (less than 10 cases per 100,000 population) - most of the regions are Center. And South America, Asia, Africa, the Caribbean.

The north and west, the higher the frequency of the disease (Moscow).

Etiology: geographic factor, viral infections, genetically determined. susceptibility.

Multifactorial theory - a combination of external fatkors acts on genetically predisposed individuals, causing chronic. Inflammation, autoimmune reactions and demyelination.

1. Genetic predisposition

- in Europeans

2. Viral infections



Pathomorphology of MS: foci of demyelination (plaque) in GM tissue (near the lateral ventricles, white matter, corpus callosum, stem structures, cerebellum).

- acute plaques - have inflammation. Changes with tissue edema and perivascular infiltration and active myelin breakdown (soft, pink)

- chronic plaques - with a prevalence of gliosis, cicatricial changes in scar tissue) - dense, gray.

Pathogenesis of MS: imbalance of the ratio of T1 to T2 cells, cytokine imbalance, expression of adhesion molecules, inclusion of cellular and humoral mechanisms, contributing to damage to the nervous tissue, generalized autoimmune reaction.

The pathogenesis of MS, see the phone. AG antigen.

Involved in the launch of autoimmune reactions. various components of myelin and proteins with antigenic properties.

Total myelin protein

Proteolipid protein

Myelin-associated.

Imbalance in the system of cytokines (protein molecules).

1. Increased production of pro-inflammatory cytokines by T1 helper cells, monocytes, glia cells in the lesion:

Lymphotoxin, interferon-gamma, necrosis factor

2. Decrease in anti-inflammatory cytokines: alpha and beta interferon, IL-4, IL-10.

Glia reaction: death of oligodendrocytes, proliferation of astrocytes, change in the functional state of astrocytes: acquisition of the immune cell in cells, production of cytokines, participation in the formation of the immune response.

See the circuit on the phone.

Maintaining the pathological process: decay products stimulate the synthesis of antibodies.
Inclusion of cellular and humoral suppressor mechanisms of suppression of autoimmune reactions: endogenous neurotrophic factors stimulating. Regenerative mechanisms - oligodendrocyte proliferation and myelination.

In the early stages, partial recovery of myelin is possible. As the disease progresses, ISM is irreversible. Form.astroglial scars. The clinical activity of the disease is not always resp. her true activity.

Clinical manifestations of MS:

The age of onset is from 15 to 59 years.

1. Symptoms of a lesion of the pyramidal tract: more often spastic. Lower paraparesis, less often hemiparesis, increased tendon reflexes, decreased abdominal reflexes, clonuses, pathological signs.

2. Damage to the cerebellum: static and dynamic. Ataxia, dysmetria, hypermetry, intentional trembling, chanted speech, macrography (large handwriting).

3. The defeat of the FMN: oculomotor., The defeat of the medial longitudinal bundle - cm internuclear ophthalmology, trigeminal, abducent, facial, nystagmus.

4. Retrobulbar neuritis: decreased or loss of vision associated with primary demyelination of the optic nerve, pain behind the eye, blurred vision, the appearance of fog, veils before the eyes, a rapid decrease in visual acuity, central scotoma, color vision impairment. After 2-3 months. spontaneous restoration of visual acuity is possible, at the fundus - blanching of the temporal halves or the entire optic nerve disc. Repeated retrobulbar neuritis is characteristic.

5. Violation of deep and superficial senses: hyposthesia, Lermitt syndrome (when the head tilted forward, a sensation of electric current along the spine arose) - damage to the posterior cords.

6. Violation of the pelvic functions: imperative urgency, increased or delayed urination, urinary incontinence. Urological complications - hydronephrosis, urosepsis - the main cause of death.

7. Mental disorders: decreased intelligence, impaired behavior, depression or euphoria.

MS is characterized by inconsistency of clinical symptoms, which is associated with the dependence of the speed of the nerve impulse on the indicators of homeostasis. The symptom of a "hot bath" is a worsening condition with an increase in body temperature. Dramatically increase.



Sharko characterized the disease as a combination of:

- lower spastic paraplegia

- intentional tremor

- speech impairment

- visual distress

- nystagmus

Symptoms of RS caused. The defeat of the pathways of GM and SM (the main target of the lesion is myelin).



Types of PC course:

1. Remmitting course - complete or incomplete recovery of functions during periods between exacerbations and the absence of an increase in symptoms during periods of remission.

2. The primary progressive course is the progression of the disease with temporary stabilization or temporary slight improvement.

3. Secondary progressive course - initially remitting current changes to progression with minimal remissions.

4. Progressive course with exacerbations-progression from the onset of the disease
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Demilienizing diseases of the nervous system. Etiology, pathogenesis, clinical forms of diseases

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